Evidence map›Paper›PMID 39198367›Full record

ArticleJournal of molecular histology2024

The GLCCI1/STAT3 pathway: a novel pathway involved in diabetic cognitive dysfunction and the therapeutic effect of salidroside.

Lin Niu, Min Xu, Wenqiang Liu, Hongdan Yu, Shengxue Yu, Fuzhi Li, Teng Wang, Die Sun, Tiefeng Yao, Wanze Li and 3 more

Abstract read
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In one paragraph

Article in Journal of molecular histology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Lin NiuDepartment of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Min Xu *Liaoning Key Laboratory of Diabetic Cognitive and Perceptive Dysfunction, Jinzhou, 121001, Liaoning, China.
Wenqiang LiuDepartment of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Hongdan YuDepartment of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Shengxue YuDepartment of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Fuzhi LiDepartment of Thoraxes Surgery of the Third Affiliated Hospital, Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Teng WangThe First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Die SunDepartment of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Tiefeng YaoDepartment of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Wanze LiDepartment of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Zhengzhong YangDepartment of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Xuezheng LiuDepartment of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, 121001, Liaoning, China. liuxuezheng@jzmu.edu.cn.
Zhongfu ZuoDepartment of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, 121001, Liaoning, China. zuozhongfu@jzmu.edu.cn.

Funding

Foundation of Education Department of Liaoning Province LJKMZ20221241Foundation of Education Department of Liaoning Province LJKZZ20220095Natural Science Foundation of Liaoning Province of China 2023-MS-312
6 · The paper itself

Abstract

Diabetic cognitive dysfunction (DCD) is a complication of diabetes that seriously affects quality of life. Glucocorticoid-induced transcript 1 (GLCCI1) has been found to be involved in inflammation, apoptosis and autophagy in various diseases. However, the distribution of GLCCI1 in the brain and its role in DCD have not yet been revealed. In addition, the potential therapeutics effects of salidroside (SAL), a phenyl propyl glycoside compound known for its neuroprotective effects in treating DCD are unknow. In the present study, we found that GLCCI1 was localized in hippocampal neurons. C57BL/6 J mice with DCD presented downregulation of GLCCI1 and Bcl-2 and upregulation of p-STAT3/STAT3, Bax, Cleaved Caspase-3/Caspase-3. Overexpression of GLCCI1 or SAL administration relieved DCD, reversed the changes in the expression of these cytokines, and alleviated morphological alterations in hippocampal neurons. Interestingly, SAL alleviated DCD and attenuated the expression of GLCCI1 and p-STAT3, showing similar effects as GLCCI1 overexpression. These findings suggest that the GLCCI1/STAT3 axis plays a crucial role in DCD and is involved in SAL-mediated attenuation of DCD.

Indexed as

Cognitive DysfunctionGlucosidesHippocampusPhenolsSignal TransductionSTAT3 Transcription FactorAnimalsApoptosisDiabetes ComplicationsDiabetes Mellitus, ExperimentalMaleMiceMice, Inbred C57BLNeuronsNeuroprotective AgentsGlucosidesNeuroprotective AgentsPhenolsrhodiolosideSTAT3 Transcription FactorApoptosisDiabetic cognitive dysfunctionGlucocorticoid-induced transcript 1Salidroside

Identifiers

PMID39198367

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.